Archives

Vitamin D Status, Type 1 Diabetes and Immune Function

By Michael McBurney

Type 1 diabetes mellitus is caused when the pancreas does not produce enough insulin. It is usually diagnosed in children and young adults. For undetermined reasons, the beta cells of the pancreas are attacked by the immune system and this leads to a complete deficiency in insulin required to transport glucose from the blood into cells of the body. The net result is that while blood glucose levels remain elevated after a meal, cells dependent upon insulin-dependent glucose transport are starved for glucose.

Federico et al (2014) studied the relationship between serum 25(OH)D levels and activity of blood immune cells against islet antigens (and measures of beta-cell function) in 15 young adolescents (12 y) with type 1 diabetes. Eight of the 15 had serum 25(OH)D levels below 20 ng/mL (50 nmol/L) and were supplemented with vitamin D to increase to levels > 50 ng/mL (125 nmol/L). After replenishing plasma vitamin D levels for 1 year, significant reductions in peripheral blood mononuclear cell reactivity against beta-cell autoantigens without any measurable changes in beta-cell function. This observational study does not establish a causal relationship of vitamin D but it does encourage further investigation into the role of serum 25(OH)D levels in modulating immunocompetent cells in individuals with type 1 diabetes.

Vitamin D is required for a healthy immune system. Low maternal serum 25(OH)D levels during pregnancy have been associated with a two-fold higher risk of type 1 diabetes in the baby (Sorensen et al, 2011). Alemzadeh et al (2008) reported that 74% of obese children and adolescents had inadequate 25(OH)D levels (< 75 nmol/L). Olson et al (2012) reported that 92% of obese and overweight children in North Texas had serum 25(OH)D levels below 75 nmol/L and 50% were below 50 nmol/L.

We need to know more about the role of serum 25(OH)D status on immune function and blood glucose management.